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Genetic architecture of gene expression underlying variation in host response to porcine reproductive and respiratory syndrome virus infection.

ABSTRACT: It has been shown that inter-individual variation in host response to porcine reproductive and respiratory syndrome (PRRS) has a heritable component, yet little is known about the underlying genetic architecture of gene expression in response to PRRS virus (PRRSV) infection. Here, we integrated genome-wide genotype, gene expression, viremia level, and weight gain data to identify genetic polymorphisms that are associated with variation in inter-individual gene expression and response to PRRSV infection in pigs. RNA-seq analysis of peripheral blood samples collected just prior to experimental challenge (day 0) and at 4, 7, 11 and 14 days post infection from 44 pigs revealed 6,430 differentially expressed genes at one or more time points post infection compared to the day 0 baseline. We mapped genetic polymorphisms that were associated with inter-individual differences in expression at each day and found evidence of cis-acting expression quantitative trait loci (cis-eQTL) for 869 expressed genes (qval?

SUBMITTER: Kommadath A

PROVIDER: S-EPMC5385538 | biostudies-literature | 2017 Apr

REPOSITORIES: biostudies-literature

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Genetic architecture of gene expression underlying variation in host response to porcine reproductive and respiratory syndrome virus infection.

Kommadath Arun A Bao Hua H Choi Igseo I Reecy James M JM Koltes James E JE Fritz-Waters Elyn E Eisley Chris J CJ Grant Jason R JR Rowland Robert R R RR Tuggle Christopher K CK Dekkers Jack C M JC Lunney Joan K JK Guan Le Luo LL Stothard Paul P Plastow Graham S GS

Scientific reports 20170410

It has been shown that inter-individual variation in host response to porcine reproductive and respiratory syndrome (PRRS) has a heritable component, yet little is known about the underlying genetic architecture of gene expression in response to PRRS virus (PRRSV) infection. Here, we integrated genome-wide genotype, gene expression, viremia level, and weight gain data to identify genetic polymorphisms that are associated with variation in inter-individual gene expression and response to PRRSV in ...[more]

PMID: 28393889

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Project description:BackgroundHigh resistance (the ability of the host to reduce pathogen load) and tolerance (the ability to maintain high performance at a given pathogen load) are two desirable host traits for producing animals that are resilient to infections. For Porcine Reproductive and Respiratory Syndrome (PRRS), one of the most devastating swine diseases worldwide, studies have identified substantial genetic variation in resistance of pigs, but evidence for genetic variation in tolerance has so far been inconclusive. Resistance and tolerance are usually considered as static traits. In this study, we used longitudinal viremia measurements of PRRS virus infected pigs to define discrete stages of infection based on viremia profile characteristics. These were used to investigate host genetic effects on viral load (VL) and growth at different stages of infection, to quantify genetic variation in tolerance at these stages and throughout the entire 42-day observation period, and to assess whether the single nucleotide polymorphism (SNP) WUR10000125 (WUR) with known large effects on resistance confers significant differences in tolerance.ResultsGenetic correlations between resistance and growth changed considerably over time. Individuals that expressed high genetic resistance early in infection tended to grow slower during that time-period, but were more likely to experience lower VL and recovery in growth by the later stage. The WUR genotype was most strongly associated with VL at early- to mid-stages of infection, and with growth at mid- to late-stages of infection. Both, single-stage and repeated measurements random regression models identified significant genetic variation in tolerance. The WUR SNP was significantly associated only with the overall tolerance slope fitted through all stages of infection, with the genetically more resistant AB pigs for the WUR SNP being also more tolerant to PRRS.ConclusionsThe results suggest that genetic selection for improved tolerance of pigs to PRRS is possible in principle, but may be feasible only with genomic selection, requiring intense recording schemes that involve repeated measurements to reliably estimate genetic effects. In the absence of such records, consideration of the WUR genotype in current selection schemes appears to be a promising strategy to improve simultaneously resistance and tolerance of growing pigs to PRRS.

Project description:Porcine Reproductive and Respiratory Syndrome (PRRS) is historically the most economically important swine disease worldwide that severely affects the reproductive performance of sows. However, little is still known about the genetic basis of reproductive performance in purebred herds during a PRRS outbreak through the comparison of maternal and terminal breeds. Thus, the objective of this work was to explore the host genetics of response to PRRS in purebred sows from two breeds. Reproductive data included 2546 Duroc and 2522 Landrace litters from 894 and 813 purebred sows, respectively, which had high-density genotype data available (29,799 single nucleotide polymorphisms; SNPs). The data were split into pre-PRRS, PRRS, and post-PRRS phases based on standardized farrow-year-week estimates. Heritability estimates for reproductive traits were low to moderate (≤0.20) for Duroc and Landrace across PRRS phases. On the other hand, genetic correlations of reproductive traits between PRRS phases were overall moderate to high for both breeds. Several associations between MARC0034894, a candidate SNP for response to PRRS, with reproductive performance were identified (P-value < 0.05). Genomic analyses detected few QTL for reproductive performance across all phases, most explaining a small percentage of the additive genetic variance (≤8.2%, averaging 2.1%), indicating that these traits are highly polygenic. None of the identified QTL within a breed and trait overlapped between PRRS phases. Overall, our results indicate that Duroc sows are phenotypically more resilient to PRRS than Landrace sows, with a similar return to PRRS-free performance between breeds for most reproductive traits. Genomic prediction results indicate that genomic selection for improved reproductive performance under a PRRS outbreak is possible, especially in Landrace sows, by training markers using data from PRRS-challenged sows. On the other hand, the high genetic correlations with reproductive traits between PRRS phases suggest that selection for improved reproductive performance in a clean environment could improve performance during PRRS, but with limited efficiency due to their low heritability estimates. Thus, we hypothesize that an indicator trait that could be indirectly selected to increase the response to selection for these traits would be desirable and would also improve the reproductive performance of sows during a PRRS outbreak.

Project description:BackgroundPorcine reproductive and respiratory syndrome (PRRS) is one of the most important swine diseases in the world and genetic selection of pigs for increased resistance to PRRS is an attractive method to improve the health status of the swine herd. This study compared phenotypic and genetic responses to infection with one of two genetically distinct type 2 PRRS virus (PRRSV) isolates: NVSL-97-7895 (NVSL) and KS-2006-72109 (KS06), and evaluated whether the single nucleotide polymorphism (SNP) WUR10000125 (WUR) on chromosome 4 that was associated with viral load and weight gain under infection with NVSL also has an effect on response to infection across North American PRRSV isolates. Wood's lactation curve was fitted to repeated viremia measurements to derive five curve characteristics that were evaluated.ResultsInfection with NVSL was characterized by reaching a 14 ± 2 % higher peak viremia (PV) 2.5 ± 0.6 days earlier (time to peak; TP) than KS06, followed by 36 ± 1 % faster virus clearance, which occurred 3.9 ± 0.7 days sooner. Weight gain from 0 to 42 days post-infection (WG) tended to be higher under infection with KS06 than NVSL (3.7 ± 1.5 kg). Estimates of heritability were moderate for both PRRSV isolates for viral load from 0 to 21 days post-infection (VL) (NVSL: 0.31 ± 0.06; KS06: 0.51 ± 0.09) and WG (NVSL: 0.33 ± 0.06; KS06: 0.31 ± 0.09). Strong negative genetic correlations were observed between VL and WG for both NVSL (-0.74 ± 0.10) and KS06 (-0.52 ± 0.17) infected pigs. Pigs with genotype AB at the WUR SNP had a more desirable phenotype than AA pigs for all traits under infection with NVSL, but only for VL and PV with KS06; effects on other traits were smaller and not significantly different from zero (P > 0.05). Genetic correlations of host response between isolates were strong for VL, WG and PV. Accounting for WUR genotype had little impact on these correlations, suggesting that response to PRRSV infection has a substantial polygenic component that is common between these two isolates.ConclusionsThese results suggest that the KS06 PRRSV isolate is less virulent than NVSL but that genetic selection for increased resistance to either of these genetically distinct isolates is expected to increase resistance to the other isolate.

Dataset Information

Genetic architecture of gene expression underlying variation in host response to porcine reproductive and respiratory syndrome virus infection.

Publications

Genetic architecture of gene expression underlying variation in host response to porcine reproductive and respiratory syndrome virus infection.

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